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Document Classification Method with Small Training Data
Yasunari MAEDA,Hideki YOSHIDA,Toshiyasu MATSUSHIMA 제어로봇시스템학회 2009 제어로봇시스템학회 국제학술대회 논문집 Vol.2009 No.8
Document classification is one of important topics in the field of NLP(Natural Language Processing). In our previous research we’ve proposed a document classification method which minimizes an error rate with reference to a Bayes criterion. But when the number of documents in training data is small, the accuracy of the previous method is low. So in this research we propose a document classification method whose accuracy is higher than the previous method when the number of documents in training data is small.
Association of a polymorphism of BTN2A1 with dyslipidemia in East Asian populations
FUJIMAKI, TETSUO,KATO, KIMIHIKO,OGURI, MITSUTOSHI,YOHIDA, TETSURO,HORIBE, HIDEKI,YOKOI, KIYOSHI,WATANABE, SACHIRO,SATOH, KEI,AOYAGI, YUKITOSHI,TANAKA, MASASHI,YOSHIDA, HIROTO,SHINKAI, SHOJI,NOZAWA, YO Spandidos Publications 2011 Experimental and therapeutic medicine Vol.2 No.4
Saeyan Choi,Bokyeong Song,Hyewon Shin,Chihyun Won,Taejoon Kim,Hideki Yoshida,Daewon Lee,Jongkyeong Chung,Kyoung Sang Cho,이임순 한국유전학회 2021 Genes & Genomics Vol.43 No.7
Background Haploinsufciency of the human nuclear receptor binding suppressor of variegation 3–9, enhancer of zeste, and trithorax (SET) domain 1 (NSD1) gene causes a developmental disorder called Sotos syndrome 1 (SOTOS1), which is associated with overgrowth and macrocephaly. NSD family proteins encoding histone H3 lysine 36 (H3K36) methyltransferases are conserved in many species, and Drosophila has a single NSD homolog gene, NSD. Objective To gain insight into the biological functions of NSD1 defciency in the developmental anomalies seen in SOTOS1 patients using an NSD-deleted Drosophila mutant. Methods We deleted Drosophila NSD using CRISPR/Cas9-mediated targeted gene knock-out, and analyzed pleiotropic phenotypes of the homozygous mutant of NSD (NSD−/−) at various developmental stages to understand the roles of NSD in Drosophila. Results The site-specifc NSD deletion was confrmed in the mutant. The H3K36 di-methylation levels were dramatically decreased in the NSD−/− fy. Compared with the control, the NSD−/− fy displayed an increase in the body size of larvae, similar to the childhood overgrowth phenotype of SOTOS1 patients. Although the NSD mutant fies survived to adulthood, their fecundity was dramatically decreased. Furthermore, the NSD−/− fy showed neurological dysfunctions, such as lower memory performance and motor defects, and a diminished extracellular signal-regulated kinase (ERK) activity. Conclusions The NSD-deleted Drosophila phenotype resembles many of the phenotypes of SOTOS1 patients, such as learning disability, deregulated ERK signaling, and overgrowth; thus, this mutant fy is a relevant model organism to study various SOTOS1 phenotypes.